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Veterans frequently need assistance because of injuries and chronic conditions, but also serve as caregivers to family and friends. Our aim was to describe the prevalence of characteristics and experiences of women veterans who serve as caregivers and compare them with non-veteran women. We measured caregiving prevalence caregiving among women veterans (N = 4,179) and women non-veterans (n = 160,307) using population-based data from 48 jurisdictions in the Behavioral Risk Factor Surveillance System from 2021 to 2022. We calculated weighted prevalence estimates and adjusted prevalence ratios [PR] for the association between veteran status and three health outcomes adjusted for age, race and ethnicity, and caregiving activities. Similar proportions (∼23%) of women veterans (n = 1,000) and non-veterans (n = 36,929) were caregivers. Among women caregivers, veterans were more likely than non-veterans to have had a chronic health condition (63 vs. 57%), disability (39 vs. 35%), and current frequent mental distress (27 vs. 22%), although all were quite prevalent in both groups. In adjusted models, the only significant difference was in current frequent mental distress among women veterans compared with non-veteran women caregivers age 18–44 (PR = 1.49, 95%CI: 1.20 − 1.85). Women veterans provide similar care as non-veteran women. However, younger women veteran caregivers more frequently experience mental distress, suggesting the importance of routine assessment of caregiving status to initiate support. This may be a result of military experiences (e.g., combat, trauma) and related comorbidities (e.g., traumatic brain injury, PTSD) that could enhance caregiving burden, making caregiver support, chronic disease self-management programs, and mental health services priorities for women veteran caregivers. [ABSTRACT FROM AUTHOR]

Objective: Epilepsy is associated with significant mortality risk. There is limited research examining how traumatic brain injury (TBI) timing affects mortality in relation to the onset of epilepsy. We aimed to assess the temporal relationship between epilepsy and TBI regarding mortality in a cohort of post‐9/11 veterans. Methods: This retrospective cohort study included veterans who received health care in the Defense Health Agency and the Veterans Health Administration between 2000 and 2019. For those diagnosed with epilepsy, the index date was the date of first antiseizure medication or first seizure; we simulated the index date for those without epilepsy. We created the study groups by the index date and first documented TBI: (1) controls (no TBI, no epilepsy), (2) TBI only, (3) epilepsy only, (4) TBI before epilepsy, (5) TBI within 6 months after epilepsy, and (6) TBI >6 months after epilepsy. Kaplan–Meier estimates of all‐cause mortality were calculated, and log‐rank tests were used to compare unadjusted cumulative mortality rates among groups compared to controls. Cox proportional hazard models were used to compute hazard ratios (HRs) with 95% confidence intervals (CIs). Results: Among 938 890 veterans, 27 436 (2.92%) met epilepsy criteria, and 264 890 (28.22%) had a TBI diagnosis. Mortality was higher for veterans with epilepsy than controls (6.26% vs. 1.12%; p <.01). Veterans with TBI diagnosed ≤6 months after epilepsy had the highest mortality hazard (HR = 5.02, 95% CI = 4.21–5.99) compared to controls, followed by those with TBI before epilepsy (HR = 4.25, 95% CI = 3.89–4.58), epilepsy only (HR = 4.00, 95% CI = 3.67–4.36), and TBI >6 months after epilepsy (HR = 2.49, 95% CI = 2.17–2.85). These differences were significant across groups. Significance: TBI timing relative to epilepsy affects time to mortality; TBI within 6 months after epilepsy or before epilepsy diagnosis was associated with earlier time to death compared to those with epilepsy only or TBI >6 months after epilepsy. [ABSTRACT FROM AUTHOR]

Previous studies have shown that a [[sigma].sup.54][[sigma].sup.s] cascade regulates the expression of a few key lipoproteins in Borrelia burgdorferi, the agent of Lyme disease. Here, we demonstrate that these sigma factors, both together and independently, regulate a much more extensive number of genes and cellular processes. Microarray analyses of [[sigma].sup.54] and [[sigma].sup.s] mutant strains identified 305 genes regulated by [[sigma].sup.54] and 145 regulated by [[sigma].sup.s] whereas the [[sigma].sup.54]-[[sigma].sup.s] regulatory cascade appears to control 48 genes in B. burgdorferi. In silico analyses revealed that nearly 80% of genes with altered expression in the [[sigma].sup.54] mutant were linked to potential [[sigma].sup.54]-dependent promoters. Many [[sigma].sup.54]-regulated genes are expressed in vivo, and through genetic complementation of the mutant, we demonstrated that [[sigma]sub.54] was required by B. burgdorferi to infect mammals. Surprisingly, [[sigma].sup.54] mutants were able to infect Ixodes scapularis ticks and be maintained for at least 24 wk after infection, suggesting the [[sigma].sup.54] [[sigma].sup.-s] regulatory network was not involved in long-term survival in ticks. However, [[sigma].sup.54] mutants did not enter the salivary glands during tick feeding, indicating that [[sigma].sup.54]-regulated genes were involved in the transmission process. infectivity | microarray | Lyme | transcription

Previous studies have shown that a σ54-σS cascade regulates the expression of a few key lipoproteins in Borrelia burgdorferi, the agent of Lyme disease. Here, we demonstrate that these sigma factors, both together and independently, regulate a much more extensive number of genes and cellular processes. Microarray analyses of σ54 and σS mutant strains identified 305 genes regulated by σ54 and 145 regulated by σS, whereas the σ54-σS regulatory cascade appears to control 48 genes in B. burgdorferi. In silico analyses revealed that nearly 80% of genes with altered expression in the σ54 mutant were linked to potential σ54-dependent promoters. Many σ54-regulated genes are expressed in vivo, and through genetic complementation of the mutant, we demonstrated that σ54 was required by B. burgdorferi to infect mammals. Surprisingly, σ54 mutants were able to infect lxodes scapularis ticks and be maintained for at least 24 wk after infection, suggesting the σ54-σS, regulatory network was not involved in long-term survival in ticks. However, σ54 mutants did not enter the salivary glands during tick feeding, indicating that σ54-regulated genes were involved in the transmission process. [ABSTRACT FROM AUTHOR]

ObjectiveMethodsResultsSignificanceTo investigate phenotypes of comorbidity before and after an epilepsy diagnosis in a national cohort of post‐9/11 Service Members and Veterans and explore phenotypic associations with mortality.Among a longitudinal cohort of Service Members and Veterans receiving care in the Veterans Health Administration (VHA) from 2002 to 2018, annual diagnoses for 26 conditions associated with epilepsy were collected over 5 years, ranging from 2 years prior to 2 years after the year of first epilepsy diagnosis. Latent class analysis (LCA) was used to identify probabilistic comorbidity phenotypes with distinct health trajectories. Descriptive statistics were used to describe the characteristics of each phenotype. Fine and Gray cause‐specific survival models were used to measure mortality outcomes for each phenotype up to 2021.Six distinct phenotypes were identified: (1) relatively healthy, (2) post‐traumatic stress disorder, (3) anxiety and depression, (4) chronic disease, (5) bipolar/substance use disorder, and (6) polytrauma. Accidents were the most common cause of death overall, followed by suicide/mental health and cancer, respectively. Each phenotype exhibited unique associations with mortality and cause of death, highlighting the differential impact of comorbidity patterns on patient outcomes.By delineating clinically meaningful epilepsy comorbidity phenotypes, this study offers a framework for clinicians to tailor interventions. Moreover, these data support systems of care that facilitate treatment of epilepsy and comorbidities within an interdisciplinary health team that allows continuity of care. Targeting treatment toward patients with epilepsy who present with specific heightened risks could help mitigate adverse outcomes and enhance overall patient care. [ABSTRACT FROM AUTHOR]

Background and Objectives: Traumatic brain injury (TBI) is a well-established epilepsy risk factor and is common among service members. Deployment-related TBI, where combat/blast may be more common, may have different outcomes than nondeployment-related TBI. This work examined associations of all TBI exposures (not just combat), and epilepsy, while adjusting for comorbidities associated with epilepsy, among veterans by deployment status., Methods: The cohort included post-9/11 veterans with ≥2 years of care in both Veterans Health Administration and Defense Health Agency systems. We identified epilepsy using ICD-9/10-CM codes, antiseizure medication, and service-connected disability for epilepsy. We conducted a logistic regression model with interaction terms for conditions by deployment history that adjusted for demographics and military characteristics., Results: The cohort (n = 938,890) included post-9/11 veterans of whom 27,436 (2.92%) had epilepsy. Most veterans had a history of deployment (70.64%), referred to as "deployed." Epilepsy was more common among veterans who were never deployed ("nondeployed") (3.85% vs 2.54%). Deployed veterans were more likely to have had TBI, compared with the nondeployed veterans (33.94% vs 14.24%), but nondeployed veterans with moderate/severe TBI had higher odds of epilepsy compared with deployed veterans (adjusted odds ratio [aOR] 2.92, 95% CI 2.68-3.17 vs aOR 2.01, 95% CI 1.91-2.11). Penetrating TBI had higher odds of epilepsy among the deployed veterans (aOR 5.33, 95% CI 4.89-5.81), whereas the odds of epilepsy for mild TBI did not significantly differ by deployment status. Although most neurologic conditions were more prevalent among the nondeployed veterans, they were often associated with higher odds of epilepsy in the deployed veterans., Discussion: Deployment history had a significant differential impact on epilepsy predictors. As expected, penetrating TBI had a greater epilepsy impact among deployed veterans perhaps due to combat/blast. Some epilepsy predictors (moderate/severe TBI, multiple sclerosis, and Parkinson disease) had a stronger association in the nondeployed veterans suggesting a potential healthy warrior effect in which such conditions preclude deployment. Other neurologic conditions (e.g., brain tumor, Alzheimer disease/frontotemporal dementia) had a greater epilepsy impact in the deployed veterans. This may be attributable to deployment-related exposures (combat injury, occupational exposures). A better understanding of deployment effects is critical to provide targeted epilepsy prevention in veterans and military service members.